There is a relationship between central nervous system missteps and markers of inflammation. Age doesn’t matter; it happens across the board. If the occasional bout of forgetfulness strikes you, you might recoil in fear of early-onset dementia, especially if the “occasions” are too close together. Is there anything you can do about this? Could it be something you ate? Maybe it’s something you didn’t eat.
Inflammation is a protective response to injury or destruction of tissue that tries to rid the body of the detrimental agent. The process elevates blood markers that are useful in predicting the onset of chronic conditions, such as diabetes or cardiovascular disease. One of these markers is called homocysteine, an amino acid made from methionine that degrades arterial architecture. But what of mental lapses? “Epidemiological studies show a positive, dose-dependent relationship between mild-to-moderate increases in plasma total homocysteine concentrations (Hcy) and the risk of neurodegenerative diseases, such as…cognitive impairment…” (Herrmann. 2011) Cognitive impairment is not necessarily a sign of impending dementia or Alzheimer’s disease, but elevated homocysteine is “…a surrogate marker for B vitamin deficiency (folate, B12, B6) and a neurotoxic agent.” (Ibid.)
If you can provide details about your forgetfulness, you don’t have dementia. If you can recall what you read yesterday about the local political scene, you don’t have dementia. If you forgot where you put the car keys, join the crowd. Nonetheless, you could have homocysteine levels that are too high for your own good. It’s recognized that taking classes, doing word puzzles, playing chess, and generally challenging the mind can preserve memory. But these activities won’t necessarily influence renegade body chemistry. Though conjectural, it has been suggested that inflammation disrupts the integrity of the blood-brain barrier, the highly selective membrane that protects the brain from pathogens in the blood, as well as regulates which molecules can pass between the blood and the cerebral spinal fluid. Inflammation compromises the function of the membrane, allowing large molecules access to the brain, resulting in neuronal damage. (Stolp. 2009).
Herrmann and Obeid (2011) admit that the prospect of improving any degree of neurological distortion caused by homocysteine can be realized with B vitamins. Parallel independent investigation revealed that women with cognitive abasement had higher Hcy values than women without such a burden, and that the folate (a B vitamin also called B9) levels of the affected cohort were measurably lower. (Faux. 2011)
Homocysteine can be changed back to methionine under the right conditions, namely in the presence of a methylation molecule, such as folic acid (called folate in food). Folate insufficiency, or outright inadequacy, can initiate mental lapses that could balloon into more serious conditions if deficit is prolonged. Therapeutically, folic acid is able to reduce Hcy and the occurrence of neural tube defects in neonates. A side benefit was observed to be the prevention of cervical dysplasia and protection against neoplasm formation in ulcerative colitis. (Kelly. 1998) Geriatric scientists had indicted homocysteine as causative of neurobehavioral anomalies across a wide range of cognitive domains (Jyme. 2005), and later identified vitamin B12, vitamin B6, and folate (or folic acid) as ameliorative agents. (Selhub. 2010)
Homocysteine levels do not always increase because of something we did or ate, but because of something we didn’t eat. That would be the foods providing ample supplies of B12, B6, and folic acid. Certain chronic and contagious diseases that evoke an inflammatory response, even the flu or seasonal allergies, can bring on a foggy mind. Relieving the cause should bring physical relief, and changing the body chemistry should eliminate the fog. All you need is a cue to help you remember that your sunglasses are sitting above your eyebrows.
Herrmann W, Obeid R. Homocysteine: a biomarker in neurodegenerative diseases. Clin Chem Lab Med. 2011 Mar;49(3):435-41.
Stolp HB, Dziegielewska KM. Review: Role of developmental inflammation and blood-brain barrier dysfunction in neurodevelopmental and neurodegenerative diseases. Neuropathol Appl Neurobiol. 2009 Apr;35(2):132-46.
Faux NG, Ellis KA, Porter L, Fowler CJ, Laws SM, Martins RN, Pertile KK, Rembach A, et al Homocysteine, Vitamin B12, and Folic Acid Levels in Alzheimer's Disease, Mild Cognitive Impairment, and Healthy Elderly: Baseline Characteristics in Subjects of the Australian Imaging Biomarker Lifestyle Study. J Alzheimers Dis. 2011 Sep 2.
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Jyme H. Schafer, MD, MPH; Thomas A. Glass, PhD; Karen I. Bolla, PhD; Margaret Mintz, MS; Anne E. Jedlicka, MS; Brian S. Schwartz, MD, MS Homocysteine and Cognitive Function in a Population-based Study of Older Adults J Am Geriatr Soc. 2005;53(3):381-388
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Aron M. Troen, Melissa Shea-Budgell, Barbara Shukitt-Hale, Donald E. Smith, Jacob Selhub, and Irwin H. Rosenberg B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice PNAS August 26, 2008 vol. 105 no. 34 12474-12479
Roberts RO, Geda YE, Knopman DS, Boeve BF, Christianson TJ, Pankratz VS, Kullo IJ, Tangalos EG, Ivnik RJ, Petersen RC. Association of C-reactive protein with mild cognitive impairment. Alzheimers Dement. 2009 Sep;5(5):398-405.
Mancinella A, Mancinella M, Carpinteri G, Bellomo A, Fossati C, Gianturco V, Iori A, Ettorre E, Troisi G, Marigliano V. Is there a relationship between high C-reactive protein (CRP) levels and dementia? Arch Gerontol Geriatr. 2009;49 Suppl 1:185-94.
Herrmann W Significance of hyperhomocysteinemia. Clin Lab. 2006;52(7-8):367-74.
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